Yellow head disease (YHD) was first described in 1991 as an epizootic in Thai shrimp farms (Limuswan 1991), and subsequent outbreaks have been reported from other shrimp farming countries in Asia. A closely related strain of YHV, named Gill-Associated virus (GAV), has been reported from Australian shrimp farms (Walker et al. 2001). Laboratory trials have shown that YHV can cause high mortality in representative cultured and wild penaeid species from the Americas (Lu et al. 1994, 1997; Lightner 1999; Pantoja & Lightner 2003). When it occurs in farms rearing P. monodon, YHD is characterized by high and rapid mortality that is sometimes accompanied by the gross signs of yellowing of the cephalothorax and general bleaching of body color from which the disease got its name. In laboratory studies, American penaeids challenged with YHV did not develop yellow heads or signs of marked discoloration (Lightner and Redman 1998). YHV is potentially lethal to most of the commercially cultivated penaeid shrimp species (OIE 2003).

The causative agent of YHD is YHV, GAV and other closely related strains of the same virus (Table 1) (OIE 2003). Transmission electron microscopy (TEM) of YHV-infected tissues shows enveloped bacilliform virions. They range from approximately 150 nm to 200 nm in length and from 40 nm to 50 nm in diameter and are located within vesicles in the cytoplasm of infected cells and in intercellular spaces. The virions arise from longer, filamentous nucleocapsids (approximately 15 nm x 130-800 nm), which accumulate in the cytoplasm and obtain an envelope by budding at the endoplasmic reticulum into intracellular vesicles. Negatively stained YHV virions show regular arrays of short spikes on the viral envelope (Figures 4 and 6) (Boonyaratpalin et al. 1993; Chantanachookin et al. 1993; Lightner 1996a).

YHV was originally described mistakenly as a granulosis-like virus (Boonyaratpalin et al. 1993; Chantanachookin et al. 1993), but it was later found to be a single-stranded, positive sense RNA (ssRNA) virus (Tang and Lightner 1999) related to nidoviruses in the Coronaviridae and Arteriviridae (Sittidilokratna et al. 2002). GAV, the Australian strain of YHV has been recognized as the type species for the new virus genus Okavirus in the new family Roniviridae (Mayo 2002a, 2002b; OIE 2003).

Although YHD was first described as an epizootic from Thai shrimp farms (Limsuwan 1991), subsequent outbreaks of YHD have been reported from cultivated shrimp in many locations in Asia (OIE 2003). YHV has also been reported in frozen imported commodity shrimp in the United States (Nunan et al. 1998; Durand et al. 2000), and it has been incorrectly reported in farmed shrimp from the Americas based on the presentation of severe necrosis of the lymphoid organ, a lesion once thought to be pathognomonic for YHD (Lightner 1996a; Lightner et al. 1998; Lightner and Redman 1998) . However, the diagnosis of YHV infection in these cases was not confirmed with a second diagnostic method until after the errant reports were published. More recent work has shown that the presumptive histological diagnoses were due to severe infections with white spot virus, which can cause histopathology in the lymphoid organ which mimics that occurring in severe acute YHD (Pantoja and Lightner 2003). Because of the risk of introduction of YHV into the Western Hemisphere with frozen commodity shrimp still remains (Nunan et al. 1998, Durand et al. 2000), and because the possibility that concurrent WSSV/YHV infections may occur, in those severe WSSV cases in which YHV infection may also be suspected, the samples should be further analyzed by another method (i.e. RT-PCR or ISH with a YHV specific probe) to confirm or rule out the presence of YHV. Hence, despite some early reports of YHV in the Americas, it has not been found infecting farmed shrimp in the Americas.

 

References:  Lightner, D. V., The Penaeid Shrimp Viral Pandemics due to IHHNV, WSSV, TSV and YHV: History in the Americas and Current Status.